PeerJ Preprints: Neurosciencehttps://peerj.com/preprints/index.atom?journal=peerj&subject=2150Neuroscience articles published in PeerJ PreprintsSeven myths on crowding and peripheral visionhttps://peerj.com/preprints/273532019-12-062019-12-06Hans Strasburger
Crowding has become a hot topic in vision research and some fundamentals are now widely agreed upon. For the classical crowding task, one would likely agree with the following statements. (1) Bouma’s law can, succinctly and unequivocally, be stated as saying that critical distance for crowding is about half the target’s eccentricity. (2) Crowding is predominantly a peripheral phenomenon. (3) Peripheral vision extends to at most 90° eccentricity. (4) Resolution threshold (the minimal angle of resolution, MAR) increases strongly and linearly with eccentricity. Crowding increases at an even steeper rate. (5) Crowding is asymmetric as Bouma has shown. For that inner-outer asymmetry, the peripheral flanker has more effect. (6) Critical crowding distance corresponds to a constant cortical distance in primary visual areas like V1. (7) Except for Bouma’s seminal paper in 1970, crowding research mostly became prominent starting in the 2000s. I propose the answer is ‘not really’ or ‘not quite’ to these assertions. So should we care? I think we should, before we write the textbook chapters for the next generation.
Crowding has become a hot topic in vision research and some fundamentals are now widely agreed upon. For the classical crowding task, one would likely agree with the following statements. (1) Bouma’s law can, succinctly and unequivocally, be stated as saying that critical distance for crowding is about half the target’s eccentricity. (2) Crowding is predominantly a peripheral phenomenon. (3) Peripheral vision extends to at most 90° eccentricity. (4) Resolution threshold (the minimal angle of resolution, MAR) increases strongly and linearly with eccentricity. Crowding increases at an even steeper rate. (5) Crowding is asymmetric as Bouma has shown. For that inner-outer asymmetry, the peripheral flanker has more effect. (6) Critical crowding distance corresponds to a constant cortical distance in primary visual areas like V1. (7) Except for Bouma’s seminal paper in 1970, crowding research mostly became prominent starting in the 2000s. I propose the answer is ‘not really’ or ‘not quite’ to these assertions. So should we care? I think we should, before we write the textbook chapters for the next generation.The investigation of 2D monolayers as potential chelation agents in Alzheimer’s diseasehttps://peerj.com/preprints/279422019-11-202019-11-20Neha PavuluruXuan Luo
In this study, we conducted Density Functional Theory calculations comparing the binding energy of the copper- Amyloid-beta complex to the binding energies of potential chelation materials. We used the first-coordination sphere of the truncated high-pH Amyloid-beta protein subject to computational limits. Binding energy and charge transfer calculations were evaluated for copper’s interaction with potential chelators: monolayer boron nitride, monolayer molybdenum disulfide, and monolayer silicene. Silicene produced the highest binding energies to copper, and the evidence of charge transfer between copper and the monolayer proves that there is a strong ionic bond present. Although our three monolayers did not directly present chelation potential, the absolute differences between the binding energies of the silicene binding sites and the Amyloid-beta binding site were minimal proving that further research in silicene chelators may be useful for therapy in Alzheimer’s disease.
In this study, we conducted Density Functional Theory calculations comparing the binding energy of the copper- Amyloid-beta complex to the binding energies of potential chelation materials. We used the first-coordination sphere of the truncated high-pH Amyloid-beta protein subject to computational limits. Binding energy and charge transfer calculations were evaluated for copper’s interaction with potential chelators: monolayer boron nitride, monolayer molybdenum disulfide, and monolayer silicene. Silicene produced the highest binding energies to copper, and the evidence of charge transfer between copper and the monolayer proves that there is a strong ionic bond present. Although our three monolayers did not directly present chelation potential, the absolute differences between the binding energies of the silicene binding sites and the Amyloid-beta binding site were minimal proving that further research in silicene chelators may be useful for therapy in Alzheimer’s disease.A lipid-invasion model for Alzheimer’s Diseasehttps://peerj.com/preprints/278112019-11-182019-11-18Jonathan D Rudge
This paper describes a potential new explanation for Alzheimer’s disease (AD), referred to here as the lipid-invasion model. It proposes that AD is primarily caused by the influx of lipids following the breakdown of the blood brain barrier (BBB). The model argues that a principal role of the BBB is to protect the brain from external lipid access. When the BBB is damaged, it allows a mass influx of (mainly albumin-bound) free fatty acids (FFAs) and lipid-rich lipoproteins to the brain, which in turn causes neurodegeneration, amyloidosis, tau tangles and other AD characteristics. The model also argues that, whilst β-amyloid causes neurodegeneration, as is widely argued, its principal role in the disease lies in damaging the BBB. It is the external lipids, entering as a consequence, that are the primary drivers of neurodegeneration in AD., especially FFAs, which induce oxidative stress, stimulate microglia-driven neuroinflammation, and inhibit neurogenesis. Simultaneously, the larger, more lipid-laden lipoproteins, characteristic of the external plasma but not the CNS, cause endosomal-lysosomal abnormalities, amyloidosis and the formation of tau tangles, all characteristic of AD. In most cases (certainly in late-onset, noninherited forms of the disease) amyloidosis and tau tangle formation are consequences of this external lipid invasion, and in many ways more symptomatic of the disease than causative. In support of this, it is argued that the pattern of damage caused by the influx of FFAs into the brain is likely to resemble the neurodegeneration seen in alcohol-related brain damage (ARBD), a disease that shows many similarities to AD, including the areas of the brain it affects. The fact that neurodegeneration is far more pronounced in AD than in ARBD, and characterised by other features, such as amyloidosis and tau tangles, most likely results from the greater heterogeneity of the lipid assault in AD compared with ethanol alone. The lipid-invasion model, described here, arguably provides the first cohesive, multi-factorial explanation of AD that accounts for all currently known major risk factors, and explains all AD-associated pathologies, including those, such as endosomal-lysosomal dysfunction and excessive lipid droplet formation, that are not well-accounted for in other explanation of this disease.
This paper describes a potential new explanation for Alzheimer’s disease (AD), referred to here as the lipid-invasion model. It proposes that AD is primarily caused by the influx of lipids following the breakdown of the blood brain barrier (BBB). The model argues that a principal role of the BBB is to protect the brain from external lipid access. When the BBB is damaged, it allows a mass influx of (mainly albumin-bound) free fatty acids (FFAs) and lipid-rich lipoproteins to the brain, which in turn causes neurodegeneration, amyloidosis, tau tangles and other AD characteristics. The model also argues that, whilst β-amyloid causes neurodegeneration, as is widely argued, its principal role in the disease lies in damaging the BBB. It is the external lipids, entering as a consequence, that are the primary drivers of neurodegeneration in AD., especially FFAs, which induce oxidative stress, stimulate microglia-driven neuroinflammation, and inhibit neurogenesis. Simultaneously, the larger, more lipid-laden lipoproteins, characteristic of the external plasma but not the CNS, cause endosomal-lysosomal abnormalities, amyloidosis and the formation of tau tangles, all characteristic of AD. In most cases (certainly in late-onset, noninherited forms of the disease) amyloidosis and tau tangle formation are consequences of this external lipid invasion, and in many ways more symptomatic of the disease than causative. In support of this, it is argued that the pattern of damage caused by the influx of FFAs into the brain is likely to resemble the neurodegeneration seen in alcohol-related brain damage (ARBD), a disease that shows many similarities to AD, including the areas of the brain it affects. The fact that neurodegeneration is far more pronounced in AD than in ARBD, and characterised by other features, such as amyloidosis and tau tangles, most likely results from the greater heterogeneity of the lipid assault in AD compared with ethanol alone. The lipid-invasion model, described here, arguably provides the first cohesive, multi-factorial explanation of AD that accounts for all currently known major risk factors, and explains all AD-associated pathologies, including those, such as endosomal-lysosomal dysfunction and excessive lipid droplet formation, that are not well-accounted for in other explanation of this disease.Software and resources for experiments and data analysis of MEG and EEG datahttps://peerj.com/preprints/279882019-10-212019-10-21Lau M. Andersen
Data from magnetoencephalography (MEG) and electroencephalography (EEG) is extremely rich and multifaceted. For example, in a standard MEG recording with 306 sensors and a sampling rate of 1,000 Hz, 306,000 data points are sampled every second. To be able to answer the question, which was the ultimate reason for acquiring the data, thus necessitates efficient data handling. Luckily, several software packages have been developed for handling MEG and/or EEG data. To name some of the most popular: MNE-Python; FieldTrip; Brainstorm; EEGLAB and SPM. These are all available under a public domain licence, meaning that they can be run, shared and modified by anyone. Commercial software released under proprietary licences include BESA and CURRY. It is important to be aware of that for clinical diagnosis of for example epilepsy, certified software is required FieldTrip, MNE-Python, Brainstorm, EEGLAB and SPM for example cannot be used for that. In this chapter, the emphasis will be on MNE-Python and FieldTrip. This will allow users of both Python and MATLAB (or alternatively GNU Octave to code along as the chapter unfolds. As a general remark, all that MNE-Python can do, FieldTrip can do and vice versa – though with some small difference. A full analysis going from raw data to a source reconstruction will be presented, illustrated with both code and figures with the aim of providing newcomers to the field a stepping stone towards doing their own analyses of their own datasets.
Data from magnetoencephalography (MEG) and electroencephalography (EEG) is extremely rich and multifaceted. For example, in a standard MEG recording with 306 sensors and a sampling rate of 1,000 Hz, 306,000 data points are sampled every second. To be able to answer the question, which was the ultimate reason for acquiring the data, thus necessitates efficient data handling. Luckily, several software packages have been developed for handling MEG and/or EEG data. To name some of the most popular: MNE-Python; FieldTrip; Brainstorm; EEGLAB and SPM. These are all available under a public domain licence, meaning that they can be run, shared and modified by anyone. Commercial software released under proprietary licences include BESA and CURRY. It is important to be aware of that for clinical diagnosis of for example epilepsy, certified software is required FieldTrip, MNE-Python, Brainstorm, EEGLAB and SPM for example cannot be used for that. In this chapter, the emphasis will be on MNE-Python and FieldTrip. This will allow users of both Python and MATLAB (or alternatively GNU Octave to code along as the chapter unfolds. As a general remark, all that MNE-Python can do, FieldTrip can do and vice versa – though with some small difference. A full analysis going from raw data to a source reconstruction will be presented, illustrated with both code and figures with the aim of providing newcomers to the field a stepping stone towards doing their own analyses of their own datasets.The effects of single versus multiple training sessions on the motor learning of two Krav Maga strike techniques, in womenhttps://peerj.com/preprints/279842019-09-252019-09-25Vincenzo E. Di BaccoMehran TaherzadehOlivier BirotWilliam H. Gage
Background. Experts of the Krav Maga (KM) self-defense system propose that KM techniques are based on simple body movements which are suggested to be learned rapidly and retained. This study investigated the acquisition, retention, and further improvement with additional training of two KM strike techniques among novice female practitioners: straight punch and defensive kick. Methods. Sixteen healthy females (age: 23 ± 3.7 years) without any previous martial arts/self-defense experience volunteered to participate. All participants received an initial 30-minute instruction session (AQ), taught by a certified KM instructor, where each technique was deconstructed into three checkpoints (defined as a component of the entire movement) for learning. Participants were divided into two groups, one of which received additional training. Several kinematic and kinetic measures were recorded at four timepoints: immediately before AQ, immediately after AQ, five days after AQ, and twelve days after AQ. Results. Results suggest that both techniques were learned rapidly, as checkpoint performance was significantly improved after AQ. Kick velocity and impact force also increased significantly after AQ, however, these measures did not change after AQ for the punch technique. Additional training did not improve either punch or kick performance beyond that learned during AQ. Conclusion. The findings from this study suggest that a single training session may be sufficient to learn and retain KM strike techniques relatively permanently; and the acquisition of the kick technique may lead to concomitant improvements in kick velocity and impact force.
Background. Experts of the Krav Maga (KM) self-defense system propose that KM techniques are based on simple body movements which are suggested to be learned rapidly and retained. This study investigated the acquisition, retention, and further improvement with additional training of two KM strike techniques among novice female practitioners: straight punch and defensive kick. Methods. Sixteen healthy females (age: 23 ± 3.7 years) without any previous martial arts/self-defense experience volunteered to participate. All participants received an initial 30-minute instruction session (AQ), taught by a certified KM instructor, where each technique was deconstructed into three checkpoints (defined as a component of the entire movement) for learning. Participants were divided into two groups, one of which received additional training. Several kinematic and kinetic measures were recorded at four timepoints: immediately before AQ, immediately after AQ, five days after AQ, and twelve days after AQ. Results. Results suggest that both techniques were learned rapidly, as checkpoint performance was significantly improved after AQ. Kick velocity and impact force also increased significantly after AQ, however, these measures did not change after AQ for the punch technique. Additional training did not improve either punch or kick performance beyond that learned during AQ. Conclusion. The findings from this study suggest that a single training session may be sufficient to learn and retain KM strike techniques relatively permanently; and the acquisition of the kick technique may lead to concomitant improvements in kick velocity and impact force.The effect of external lateral stabilization on the use of foot placement to control mediolateral stability in walking and runninghttps://peerj.com/preprints/272442019-09-202019-09-20Mohammadreza MahakiSjoerd M BruijnJaap H. van Dieën
It is still unclear how humans control mediolateral (ML) stability in walking and even more so for running. Here, foot placement strategy as a main mechanism to control ML stability was compared between walking and running. Moreover, to verify the role of foot placement as a means to control ML stability in both modes of locomotion, this study investigated the effect of external lateral stabilization on foot placement control. Ten young adults participated in this study. Kinematic data of the trunk (T6) and feet were recorded during walking and running on a treadmill in normal and stabilized conditions. Correlation between ML trunk CoM state and subsequent ML foot placement, step width, and step width variability were assessed. Paired t-tests (either SPM1d or normal) were used to compare aforementioned parameters between normal walking and running. Two-way repeated measures ANOVAs (either SPM1d or normal) were used to test for effects of walking vs. running and of normal vs. stabilized condition. We found a stronger correlation between ML trunk CoM state and ML foot placement and significantly higher step width and step width variability in walking than in running. The correlation between ML trunk CoM state and ML foot placement, step width, and step width variability were significantly decreased by external lateral stabilization in walking and running, and this reduction was stronger in walking than in running. We conclude that ML foot placement is coordinated to ML trunk CoM state to stabilize both walking and running and this coordination is stronger in walking than in running.
It is still unclear how humans control mediolateral (ML) stability in walking and even more so for running. Here, foot placement strategy as a main mechanism to control ML stability was compared between walking and running. Moreover, to verify the role of foot placement as a means to control ML stability in both modes of locomotion, this study investigated the effect of external lateral stabilization on foot placement control. Ten young adults participated in this study. Kinematic data of the trunk (T6) and feet were recorded during walking and running on a treadmill in normal and stabilized conditions. Correlation between ML trunk CoM state and subsequent ML foot placement, step width, and step width variability were assessed. Paired t-tests (either SPM1d or normal) were used to compare aforementioned parameters between normal walking and running. Two-way repeated measures ANOVAs (either SPM1d or normal) were used to test for effects of walking vs. running and of normal vs. stabilized condition. We found a stronger correlation between ML trunk CoM state and ML foot placement and significantly higher step width and step width variability in walking than in running. The correlation between ML trunk CoM state and ML foot placement, step width, and step width variability were significantly decreased by external lateral stabilization in walking and running, and this reduction was stronger in walking than in running. We conclude that ML foot placement is coordinated to ML trunk CoM state to stabilize both walking and running and this coordination is stronger in walking than in running.Identifying the spatial frequency specific orientation aftereffect in the visual systemhttps://peerj.com/preprints/279732019-09-202019-09-20Hiran Perera-W.A.
Previous studies have found that feature selectivity such as orientation and spatial frequency predominantly involves cortical mechanisms, and decades of research have identified the presence of orientation and spatial frequency-specific channels in the cortical region. Prolonged exposure to stimuli will generate an adapting aftereffect, thus reducing the neural sensitivity of those channels. Based on that notion, this research aims to identify whether the visual system encodes orientation variance independent of spatial frequency. Two experiments were conducted to assess the outcome of the study. In experiment 1, subjects viewed the stimuli with both eyes, and in experiment 2, stimuli were presented to one eye and viewed from the same or the contralateral eye. Results from both experiments indicated no interaction effect between spatial frequency and orientation aftereffect. Thus, supporting the experiments that orientation and spatial frequency are separately coded in the visual system.
Previous studies have found that feature selectivity such as orientation and spatial frequency predominantly involves cortical mechanisms, and decades of research have identified the presence of orientation and spatial frequency-specific channels in the cortical region. Prolonged exposure to stimuli will generate an adapting aftereffect, thus reducing the neural sensitivity of those channels. Based on that notion, this research aims to identify whether the visual system encodes orientation variance independent of spatial frequency. Two experiments were conducted to assess the outcome of the study. In experiment 1, subjects viewed the stimuli with both eyes, and in experiment 2, stimuli were presented to one eye and viewed from the same or the contralateral eye. Results from both experiments indicated no interaction effect between spatial frequency and orientation aftereffect. Thus, supporting the experiments that orientation and spatial frequency are separately coded in the visual system.Vocal emotion recognition in school-age children: normative data for the EmoHI testhttps://peerj.com/preprints/279212019-08-282019-08-28Leanne NagelsEtienne GaudrainDebi VickersMarta Matos LopesPetra HendriksDeniz Başkent
Traditionally, emotion recognition research has primarily used pictures and videos while audio test materials have received less attention and are not always readily available. Particularly for testing vocal emotion recognition in hearing-impaired listeners, the audio quality of assessment materials may becrucial. Here, we present a vocal emotion recognition test with non-language specific pseudospeech productions of multiple speakers expressing three core emotions (happy, angry, and sad): the EmoHI test. Recorded with high sound quality, the test is suitable to use with populations of children and adults with normal or impaired hearing, and across different languages. In the present study, we obtained normative data for vocal emotion recognition development in normal-hearing school-age (4-12 years) children using the EmoHI test. In addition, we tested Dutch and English children to investigate cross-language effects. Our results show that children’s emotion recognition accuracy scores improved significantly with age from the youngest group tested on (mean accuracy 4-6 years: 48.9%), but children’s performance did not reach adult-like values (mean accuracy adults: 94.1%) even for the oldest age group tested (mean accuracy 10-12 years: 81.1%). Furthermore, the effect of age on children’s development did not differ across languages. The strong but slow development in children’s ability to recognize vocal emotions emphasizes the role of auditory experience in forming robust representations of vocal emotions. The wide range of age-related performances that are captured and the lack of significant differences across the tested languages affirm the usability and versatility of the EmoHI test.
Traditionally, emotion recognition research has primarily used pictures and videos while audio test materials have received less attention and are not always readily available. Particularly for testing vocal emotion recognition in hearing-impaired listeners, the audio quality of assessment materials may becrucial. Here, we present a vocal emotion recognition test with non-language specific pseudospeech productions of multiple speakers expressing three core emotions (happy, angry, and sad): the EmoHI test. Recorded with high sound quality, the test is suitable to use with populations of children and adults with normal or impaired hearing, and across different languages. In the present study, we obtained normative data for vocal emotion recognition development in normal-hearing school-age (4-12 years) children using the EmoHI test. In addition, we tested Dutch and English children to investigate cross-language effects. Our results show that children’s emotion recognition accuracy scores improved significantly with age from the youngest group tested on (mean accuracy 4-6 years: 48.9%), but children’s performance did not reach adult-like values (mean accuracy adults: 94.1%) even for the oldest age group tested (mean accuracy 10-12 years: 81.1%). Furthermore, the effect of age on children’s development did not differ across languages. The strong but slow development in children’s ability to recognize vocal emotions emphasizes the role of auditory experience in forming robust representations of vocal emotions. The wide range of age-related performances that are captured and the lack of significant differences across the tested languages affirm the usability and versatility of the EmoHI test.KCNMA1-linked channelopathyhttps://peerj.com/preprints/278762019-08-192019-08-19Cole S BaileyHans J MoldenhauerSu Mi ParkSotirios KerosAndrea L Meredith
KCNMA1 encodes the pore-forming α subunit of the ‘Big K+’ (BK) large conductance calcium and voltage-activated K+ channel. BK channels are widely distributed across tissues, including both excitable and non-excitable cells. Expression levels are highest in brain and muscle, where BK channels are critical regulators of neuronal excitability and muscle contractility. A global deletion in mouse (KCNMA1–/–) is viable but exhibits pathophysiology in many organ systems. Yet despite the important roles in animal models, the consequences of dysfunctional BK channels in humans are not well-characterized. Here, we summarize 16 rare KCNMA1 mutations identified in 37 patients dating back to 2005, with an array of clinically defined pathological phenotypes collectively referred to as ‘KCNMA1-linked channelopathy.’ These mutations encompass gain-of-function (GOF) and loss-of-function (LOF) alterations in BK channel activity, as well as several variants of unknown significance (VUS). Human KCNMA1 mutations are primarily associated with neurological conditions, including seizures, movement disorders, developmental delay, and intellectual disability. Due to the recent identification of additional patients, the spectrum of symptoms associated with KCNMA1 mutations has expanded but remains primarily defined by brain and muscle dysfunction. Emerging evidence suggests the functional BK channel alterations produced by different KCNMA1 alleles may associate with semi-distinct patient symptoms, such as paroxysmal non-kinesigenic dyskinesia (PNKD) with GOF and ataxia with LOF. However, due to the de novo origins for the majority of KCNMA1 mutations identified to date, and the phenotypic variability exhibited by patients, additional evidence is required to establish causality in most cases. The symptomatic picture developing from patients with KCNMA1-linked channelopathy highlights the importance of better understanding the roles BK channels play in regulating cell excitability. Establishing causality between KCNMA1-linked BK channel dysfunction and specific patient symptoms may reveal new treatment approaches with the potential to increase therapeutic efficacy over current standard regimens.
KCNMA1 encodes the pore-forming α subunit of the ‘Big K+’ (BK) large conductance calcium and voltage-activated K+ channel. BK channels are widely distributed across tissues, including both excitable and non-excitable cells. Expression levels are highest in brain and muscle, where BK channels are critical regulators of neuronal excitability and muscle contractility. A global deletion in mouse (KCNMA1–/–) is viable but exhibits pathophysiology in many organ systems. Yet despite the important roles in animal models, the consequences of dysfunctional BK channels in humans are not well-characterized. Here, we summarize 16 rare KCNMA1 mutations identified in 37 patients dating back to 2005, with an array of clinically defined pathological phenotypes collectively referred to as ‘KCNMA1-linked channelopathy.’ These mutations encompass gain-of-function (GOF) and loss-of-function (LOF) alterations in BK channel activity, as well as several variants of unknown significance (VUS). Human KCNMA1 mutations are primarily associated with neurological conditions, including seizures, movement disorders, developmental delay, and intellectual disability. Due to the recent identification of additional patients, the spectrum of symptoms associated with KCNMA1 mutations has expanded but remains primarily defined by brain and muscle dysfunction. Emerging evidence suggests the functional BK channel alterations produced by different KCNMA1 alleles may associate with semi-distinct patient symptoms, such as paroxysmal non-kinesigenic dyskinesia (PNKD) with GOF and ataxia with LOF. However, due to the de novo origins for the majority of KCNMA1 mutations identified to date, and the phenotypic variability exhibited by patients, additional evidence is required to establish causality in most cases. The symptomatic picture developing from patients with KCNMA1-linked channelopathy highlights the importance of better understanding the roles BK channels play in regulating cell excitability. Establishing causality between KCNMA1-linked BK channel dysfunction and specific patient symptoms may reveal new treatment approaches with the potential to increase therapeutic efficacy over current standard regimens.Reproducible research into human semiochemical cues and pheromones: learning from psychology’s renaissancehttps://peerj.com/preprints/279082019-08-192019-08-19Tristram D Wyatt
As with other mammals, smell in the form of semiochemicals is likely to influence the behaviour of humans, as olfactory cues to emotions, health, and mate choice. A subset of semiochemicals, pheromones, chemical signals within a species, have been identified in many mammal species. As mammals, we may have pheromones too. Sadly, the story of molecules claimed to be ‘putative human pheromones’ is a classic example of bad science carried out by good scientists. Much of human semiochemicals research including work on ‘human pheromones’ and olfactory cues comes within the field of psychology. Thus, the research is highly likely to be affected by the ‘reproducibility crisis’ in psychology and other life sciences. Psychology researchers have responded with proposals to enable better, more reliable science, with an emphasis on enhancing reproducibility. A key change is the adoption of study pre-registration which will also reduce publication bias. Human semiochemicals research would benefit from adopting these proposals.
As with other mammals, smell in the form of semiochemicals is likely to influence the behaviour of humans, as olfactory cues to emotions, health, and mate choice. A subset of semiochemicals, pheromones, chemical signals within a species, have been identified in many mammal species. As mammals, we may have pheromones too. Sadly, the story of molecules claimed to be ‘putative human pheromones’ is a classic example of bad science carried out by good scientists. Much of human semiochemicals research including work on ‘human pheromones’ and olfactory cues comes within the field of psychology. Thus, the research is highly likely to be affected by the ‘reproducibility crisis’ in psychology and other life sciences. Psychology researchers have responded with proposals to enable better, more reliable science, with an emphasis on enhancing reproducibility. A key change is the adoption of study pre-registration which will also reduce publication bias. Human semiochemicals research would benefit from adopting these proposals.